Purinergic Signalling in Pancreatic Islet Endothelial Cells - Extracellular ATP and Adenosine as Regulators of Endothelial Cell Function - page 215

Fig. 12.3 Percentage alterations of the diameter in an arteriole, associated with an isolated
islet, during step-by-step increase of ATP in 2-min intervals. The experiment was performed as
previously described [51]

12.4 Interactions Between Endocrine Cells and Islet
Endothelium

12.4.1 External ATP is a Regulator of Ca 2+ Rises Triggering
Pulsatile Insulin Release

Each -cell is a biological oscillator responding to a glucose stimulus with peri-

odic depolarization and accompanying entry of Ca 2+ . It is generally accepted that
the resulting [Ca 2+ ] i oscillations are the main trigger for pulses of insulin release
[36]. A key factor for the depolarization is closure of K + channels mediated by the
increase of cytoplasmic ATP. Within the pancreas, the

β

-cells will be entrained into
a common rhythm both by gap junctions [5] and diffusible messengers, such as
ATP [30, 35]. The coordinating action of external ATP is supposed to be mediated
by generation of IP 3 -induced increases (transients) of [Ca 2+ ] i , which temporarily
interrupt the entry of Ca 2+ by activating a repolarizing K + current [22]. Pancreatic
β

β

-cells are both recipients of coordinating ATP signals, and release this nucleotide
intermittently through exocytosis [32, 75]. The prerequisite for cyclic variations of
circulating insulin is that [Ca 2+ ] i oscillations in the -cells appear in the same phase.

It is likely that neural activity with discharge of ATP accounts for the entrainment
of the islets into common rhythm [28].

β